Freemont A J
Tissue Injury and Repair Research Group, Research School of Clinical and Laboratory Sciences, University of Manchester, Manchester, UK.
Rheumatology (Oxford). 2009 Jan;48(1):5-10. doi: 10.1093/rheumatology/ken396. Epub 2008 Oct 14.
In 2007, three times as many peer reviewed publications covering the biology and biotherapeutics of intervertebral disc (IVD) disease appeared in the literature than in 1997. This is testimony to the upsurge in interest in the IVD, mainly driven by the openings that modern molecular pathology has generated to investigate mechanisms of human disease and the potential offered by novel therapeutic technologies to use data coming from these studies to positively influence chronic discogenic back pain and sciatica. Molecular pathology has shown IVD degeneration, a major cause of low back pain, to be a complex, active disorder in which disturbed cytokine biology, cellular dysfunction and altered load responses play key roles. This has translated into a search for target molecules and disease processes that might be the focus of future, evidence-based therapies for back pain. It is not possible to describe the totality of advances that have been made in understanding the biology of the IVD in recent years, but in this review those areas of biology that are currently influencing, or could conceivably soon impinge on, clinical thinking or practice around IVD degeneration and discogenic back pain are described and discussed.
2007年，发表在文献中的、经同行评审的关于椎间盘（IVD）疾病生物学和生物治疗学的出版物数量是1997年的三倍。这证明了人们对IVD兴趣的激增，主要是由现代分子病理学为研究人类疾病机制所带来的契机以及新型治疗技术利用这些研究数据对慢性椎间盘源性背痛和坐骨神经痛产生积极影响的潜力所推动的。分子病理学表明，IVD退变作为腰痛的主要原因，是一种复杂的、活跃的病症，其中细胞因子生物学紊乱、细胞功能障碍和负荷反应改变起着关键作用。这已转化为对可能成为未来基于证据的背痛治疗靶点分子和疾病过程的探索。不可能描述近年来在理解IVD生物学方面取得的所有进展，但在本综述中，将描述和讨论目前正在影响或可能很快影响围绕IVD退变和椎间盘源性背痛的临床思维或实践的生物学领域。
